RETRACTED ARTICLE: Long Non-coding RNA MALAT1/microRNA-143/VEGFA Signal Axis Modulates Vascular Endothelial Injury-Induced Intracranial Aneurysm

Gao, Ge; Zhang, Yang; Yu, Jian; Chen, Yu; Gu, Daqun; Niu, Chaoshi; Fu, Xianming; Wei, Jian‐Jun

doi:10.1186/s11671-020-03357-2

Cited by 17 publications

(15 citation statements)

References 30 publications

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“…In addition, it has previously been discussed that cluster miR-143/miR-145 takes part in various biological processes associated with IA formation and the expression cluster miR-143/miR-145 is downregulated in IA tissues [65]. Gao et al in their study showed that lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) and VEGF-A are upregulated and miR-143 is downregulated in IA tissues (rat models of IA and IA patients) [66]. Moreover, the authors demonstrated that a decrease in MALAT1 expression induced by short hairpin RNA (sh)-MALAT1 interference inhibited apoptosis and promoted the viability of ECs in IA by modulating miR-143/VEGF-A axis.…”

Section: Lncrna-based Therapeuticsmentioning

confidence: 99%

The Role of Long Non-Coding RNAs in Intracranial Aneurysms and Subarachnoid Hemorrhage

Gareev

Beylerli

Aliev

et al. 2020

Life

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Intracranial aneurysms (IAs) represent the most complex and relevant problem of modern neurology and neurosurgery. They serve as one of the main causes of non-traumatic subarachnoid hemorrhage (SAH), causing up to 85% of all cases of intracranial hemorrhage, which is associated with frequent disability and high mortality among patients. Unfortunately, the molecular mechanisms of the development and rupture of IAs are still under study. Long non-coding RNAs (lncRNAs) are non-coding RNAs that typically have a length of more than 200 nucleotides. It is known that lncRNAs regulate many processes, such as transcription, translation, cell differentiation, regulation of gene expression, and regulation of the cell cycle. In recent years, a lot of evidence has established their role in human diseases from oncology to cardiovascular disease. Recent studies have shown that lncRNAs may be involved in the pathogenesis of IAs. The study of lncRNAs and its targets in various pathological conditions of a person is a rapidly developing field, and it is likely that the knowledge obtained from these studies regarding the pathogenesis of intracranial aneurysms will have the potential to use lncRNAs in therapy, as well as in the diagnosis and prediction of high aneurysms risk of rupture.

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Section: Lncrna-based Therapeuticsmentioning

confidence: 99%

The Role of Long Non-Coding RNAs in Intracranial Aneurysms and Subarachnoid Hemorrhage

Gareev

Beylerli

Aliev

et al. 2020

Life

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“…Endothelial cells are the main cell type of blood vessels and involved in the process of vascular morphogenesis, homeostasis and diseases [6]. Endothelial cell injury resulted by in ammation has been reported to be involved in the development of diseases, including atherosclerosis, cerebral aneurysm and IAs [7][8][9]. In addition, increasing studies have demonstrated that endothelial cell senescence and functional alterations also play important roles in vascular diseases.…”

Section: Introductionmentioning

confidence: 99%

LncRNA-ADAM11 regulates the vascular endothelial cell senescence and promotes the development of intracranial aneurysm via MiR-223-3p/NLRP3 pathway

Yong

Yan

Zhou

et al. 2022

Preprint

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Intracranial aneurysms (IAs) are the localized dilatations of intracranial arteries because of the weaknesses of the endothelial layer. It causes subarachnoid hemorrhage (SAH), which accounted for 80% of total SAH and has 50% fatality rate. Cell senescence, especially endothelial cells senescence, is closely related to the occurrence of vascular diseases. However, the relationship of endothelial cell senescence and IAs have not well defined. It is reported that circulating exosomes and exosomes-derived lncRNAs involved in the process of various diseases. LncRNAs expression aberrant in serum and IAs tissues from IA patients has been confirmed. However, the relationship of serum exosomes-derived lncRNAs and endothelial cell senescence in IAs has unclearly. Therefore, the current study aims to investigate the roles and underlying mechanisms of circulating exosomes-derived lncRNA in the senescent endothelial cells of IAs. In this study, we used ligation operation to construct IA rats. We also isolated and cultured endothelial cells from rat’s ACA/OA bifurcation. The blood pressure was detected to confirm the IA rats construction. HE staining and SA-β-gal staining was used to detect the pathologic of aneurysm and cell senescence. The expression of senescence marker genes and NLRP3 inflammasome-related genes was detected by western blot. ELISA was used to detect the expression levels of inflammatory factor. Immunofluorescence was used to confirm the cell type of senescence. Differential expression lncRNAs were identified by RNA sequencing in exosomes from clinical samples. Exosomes-derived lncRNA function was confirmed through co-culture and overexpression or knockdown lncRNA. Luciferase reporter assay and RIP assay confirmed the target binding of miRNA and lncRNA. Rescue experiments were performed to confirm lncRNA-miRNA-mRNA mechanism in endothelial cell senescence. The present study found that NLRP3 involved in the process of endothelial cell senescence in IAs. Exosomes from IA patient’s peripheral blood promoted endothelial cells senescence through transferring lncRNA ADAM11. In mechanism, lncADAM11 promoted endothelial cells senescence through competing bind to miR-223-3p and further promoting the expression of NLRP3. In conclusion, circulating exosomes-derived lncRNA ADAM11 regulated the senescence of vascular endothelial cells and promoted the development of IA via miR-223-3p/NLRP3 axis.

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“… 10 For instance, lncRNAs and miRNAs affect protein production and regulate other noncoding RNAs to regulate IA growth and rupture. 11 , 12 Although lacking protein-coding capacity, lncRNAs and miRNAs participate in human diseases, including IA, mainly by affecting the expression of protein-coding genes. Therefore, regulating the expression of certain miRNAs or lncRNAs with critical functions in IA may provide potentials for IA treatment.…”

Section: Introductionmentioning

confidence: 99%

“…Therefore, regulating the expression of certain miRNAs or lncRNAs with critical functions in IA may provide potentials for IA treatment. 11 , 12 …”

Section: Introductionmentioning

confidence: 99%

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LncRNA SAMMSON Overexpression Suppresses Vascular Smooth Muscle Cell Proliferation via Inhibiting miR-130a Maturation to Participate in Intracranial Aneurysm

Pan

Gao

Wan

et al. 2021

NDT

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Background MiR-130a is a recently identified critical player in vascular smooth muscle cell (VSMC) proliferation, which participates in intracranial aneurysm (IA). However, the involvement of miR-130a in IA and its upstream regulator are unknown. Our preliminary sequencing analysis revealed a close correlation between miR-130a and lncRNA SAMMSON across IA samples. Therefore, we further studied the crosstalk between SAMMSON and miR-130a in IA. Methods SAMMSON and miR-130a expression were measured using RT-qPCR. SAMMSON subcellular location was analyzed with nuclear fractionation assay. Their direct interaction was explored with RNA pull-down assay. The role of SAMMSON in miR-130a maturation was studied with overexpression analysis. VSMC cell proliferation was analyzed with BrdU assay. Results SAMMSON and premature miR-130a were deregulated in IA, while mature miR-130a was upregulated in IA. SAMMSON is localized in both the nucleus and cytoplasm, and direct interaction between SAMMSON and miR-130a was observed. SAMMSON overexpression suppressed miR-130a maturation in VSMCs and reduced the enhancing effects of miR-130a on VSMC cell proliferation. Conclusion SAMMSON is overexpressed in IA and suppresses VSMC proliferation via inhibiting miR-130a maturation.

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RETRACTED ARTICLE: Long Non-coding RNA MALAT1/microRNA-143/VEGFA Signal Axis Modulates Vascular Endothelial Injury-Induced Intracranial Aneurysm

Cited by 17 publications

References 30 publications

The Role of Long Non-Coding RNAs in Intracranial Aneurysms and Subarachnoid Hemorrhage

The Role of Long Non-Coding RNAs in Intracranial Aneurysms and Subarachnoid Hemorrhage

LncRNA-ADAM11 regulates the vascular endothelial cell senescence and promotes the development of intracranial aneurysm via MiR-223-3p/NLRP3 pathway

LncRNA SAMMSON Overexpression Suppresses Vascular Smooth Muscle Cell Proliferation via Inhibiting miR-130a Maturation to Participate in Intracranial Aneurysm

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